Abstract
An experimental model of brainstem ischemia was developed by embolization technique with cylindrical silicone rubber emboli in cats. The embolus reached the basilar artery in 55 cats (58.5%) and stopped in the upper basilar artery (UB) in 32, the middle basilar artery (MB) in 22 and the lower basilar artery (LB) in one animal. When the basilar artery distal to the embolus was not visualized (type 1) by postoperative vertebral angiogram, Evans blue extravasation was observed in the brainstem caudal to the embolus. When only a filling defect of the basilar artery at the site of the embolus was noted (type 2), dye extravasation was observed in the brainstem around the site of the embolus. In UB type 1, the regional cerebral blood flow of pons and medulla oblongata decreased immediately after embolization, and six hours after embolization it was 11.4 +/- 5.7 (pons) and 11.7 +/- 4.6 ml/100 g/min (medulla oblongata). In UB type 1 and MB type 1 animals, coma, apnea, tetraplegia, and disturbance of swallowing were noted. These animals died within 50 hours after embolization. Animals of UB type 2 and MB type 2 showed neurological deficits, but survived for three days. This paper discusses this method of producing experimental brainstem ischemia, the sites of ischemic lesions, and clinicopathological findings.
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